The inhibition of Aβ peptide development and aggregation is a hopeful curative approach for the discovery of disease modifying drugs for Alzheimer's disease (AD) treatment. Recent research mainly focuses on the discovery of drugs from marine setting due to their immense therapeutic potential. The present study aims to evaluate the brown macroalga Padina gymnospora and its active constituent α-bisabolol against Aβ25-35 induced neurotoxicity in Neuro2a cells and transgenic Caenorhabditis elegans (CL2006 and CL4176). The results of the in vitro study revealed that the acetone extract of P. gymnospora (ACTPG) and its active constituent α-bisabolol restores the Aβ25-35 induced alteration in the oxidation of intracellular protein and lipids. In addition, ACTPG and α-bisabolol inhibited cholinesterase and β-secretase activity in Neuro2a cells. Moreover, the intracellular reactive oxygen species (ROS) and reactive nitrogen species (RNS) production was reduced by ACTPG and α-bisabolol in Neuro2a cells. The decrease in the expression level of apoptotic proteins such as Bax and caspase-3 in ACTPG and α-bisabolol treated group indicates that the seaweed and its bioactive compound have anti-apoptotic property. Further, the in vivo study revealed that the ACTPG and α-bisabolol exerts neuroprotective effect against Aβ induced proteotoxicity in transgenic C. elegans strains of AD. Moreover it altered the Aβ mediated pathways, lifespan, macromolecular damage and down regulated the AD related gene expression of ace-1, hsp-4 and Aβ, thereby preventing Aβ synthesis. Overall, the outcome of the study signifies the neuroprotective effect of ACTPG and α-bisabolol against Aβ mediated AD pathology.

中文翻译：

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在 Neuro2a 细胞和转基因秀丽隐杆线虫阿尔茨海默病模型中，裸孢粉藻（褐藻科）及其活性成分 α-红没药醇可抑制淀粉样蛋白 - β 诱导的神经病理学作用。


抑制 Aβ 肽的发育和聚集是发现治疗阿尔茨海默病 (AD) 的疾病修饰药物的一种有希望的治疗方法。最近的研究主要集中在从海洋环境中发现药物，因为它们具有巨大的治疗潜力。本研究旨在评估棕色大型藻裸孢子藻及其活性成分 α-红没药醇对 Aβ25-35 诱导的 Neuro2a 细胞和转基因秀丽隐杆线虫（CL2006 和 CL4176）神经毒性的作用。体外研究结果表明，裸孢假单胞菌丙酮提取物 (ACTPG) 及其活性成分 α-红没药醇可恢复 Aβ25-35 诱导的细胞内蛋白质和脂质氧化的改变。此外，ACTPG 和 α-红没药醇抑制 Neuro2a 细胞中的胆碱酯酶和 β-分泌酶活性。此外，在 Neuro2a 细胞中，ACTPG 和 α-红没药醇减少了细胞内活性氧 (ROS) 和活性氮 (RNS) 的产生。 ACTPG和α-红没药醇治疗组中凋亡蛋白如Bax和caspase-3表达水平的降低表明海藻及其生物活性化合物具有抗凋亡特性。此外，体内研究表明，ACTPG 和 α-红没药醇对 AD 转基因线虫菌株中 Aβ 诱导的蛋白毒性发挥神经保护作用。此外，它还改变了Aβ介导的途径、寿命、大分子损伤，并下调了AD相关基因ace-1、hsp-4和Aβ的表达，从而阻止了Aβ的合成。总体而言，该研究的结果表明 ACTPG 和 α-红没药醇对 Aβ 介导的 AD 病理具有神经保护作用。